Abstract

Recently, catheter-based renal denervation (RDN) has become available. In order to understand better the possible role of RDN as a treatment modality, we first discuss the anatomy and function of the renal nerves in this brief review. Secondly, we address the question - what is the clinical evidence for the involvement of the kidneys and renal nerves in the pathogenesis of sympathetic hyperactivity. Finally, we will discuss how this sympathetic hyperactivity can be reduced, specifically addressing the possible role of RDN.

Questions/Answers

Sebastian Ewen: Do you measure the sympathetic activity in patients with resistant hypertension?

Peter J. Blankestijn: Ideally the answer is "yes". However, quantifying sympathetic activity is difficult. Tracer spillover techniques and muscle sympathtic nerve activity (MSNA) are considered more or less "gold standard" methods. Both methods are unsuitable for use in every day clinics. There is great need for methods of quantifying sympathetic activity on a more simple way, which are also predictors of the effect of RDN. One such method could be urinary output of catecholamine metabolites. Research needs to be done in this field.

Sebastian Ewen: What is the pathophysiological key mechanism of renal denervation?

Peter J. Blankestijn: That is a very good question and presently unknown. My hypothesis would be that disruption of the renal nerves causes peripheral resistance to drop (and possibly renal salt sensitivity to change).

Sebastian Ewen: Where do you see further indications for renal denervation based on the pathophysiological backround?